Targeting Bone Marrow-Derived Fibroblasts for Renal Fibrosis

被引:9
|
作者
An, Changlong [1 ,2 ,3 ,4 ]
Jia, Li [3 ,4 ]
Wen, Jia [1 ,3 ,4 ]
Wang, Yanlin [1 ,2 ,3 ,4 ]
机构
[1] Univ Connecticut, Ctr Hlth, Dept Med, Div Nephrol, Farmington, CT 06030 USA
[2] Vet Affairs Connecticut Healthcare Syst, Renal Sect, West Haven, CT USA
[3] Baylor Coll Med, Selzman Inst Kidney Hlth, Houston, TX 77030 USA
[4] Baylor Coll Med, Dept Med, Nephrol Sect, Houston, TX 77030 USA
来源
关键词
Chemokine; Cytokine; Bone marrow-derived fibroblast precursors; Fibroblasts; Renal fibrosis; Extracellular matrix; Chronic kidney disease; Monocyte-to-fibroblast transition; TRANSMEMBRANE CXC-CHEMOKINE; TUMOR-NECROSIS-FACTOR; CD4(+) T-CELLS; CIRCULATING FIBROCYTES; MYOFIBROBLAST POPULATION; CARDIAC INFLAMMATION; EXPRESSION CLONING; SCAVENGER RECEPTOR; KIDNEY INJURY; ADIPONECTIN;
D O I
10.1007/978-981-13-8871-2_14
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Renal fibrosis is a major pathological feature of chronic kidney disease, which is characterized by massive fibroblast activation and excessive production and deposition of extracellular matrix (ECM). Renal fibrosis results in progressive loss of kidney function; however, there is currently no effective therapy available clinically to treat or even reverse renal fibrosis. Although activated fibroblasts/myofibroblasts are responsible for the production and deposition of ECM, their origin has been debatable. Recent studies have provided compelling evidence that bone marrow-derived fibroblast precursors contribute significantly to the population of myofibroblasts and the development of renal fibrosis. Therefore, targeting the molecular signaling mechanisms underlying the recruitment and activation of the bone marrow-derived fibroblast precursors may serve as novel therapeutic strategy for chronic kidney disease. In this review, we appraise recent advances in our understanding of the recruitment and activation of bone marrow-derived fibroblast precursors in the kidney and the development of renal fibrosis and highlight novel molecular signaling pathways that may lead to the development of new therapies for chronic kidney disease.
引用
收藏
页码:305 / 322
页数:18
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